Here is a case that is about 12 months old. The right central incisor had a history of trauma and at the consultation appointment there were clinical signs of infection (chronic apical abscess).

By the time I saw the child for treatment, the apical lesion had enlarged. The plan for treatment was endodontic therapy, of course, but I was unsure if apexification would be necessary. I assumed it would be, but decided to play things by eye.

Once I got into the tooth I found pus in the coronal third of the canal but as I worked my way further up the canal, hyperemia developed. The apically vital pulp was likely the reason that I found an apical stop.

The apical vitality and stop allowed me to complete the case, rather than medicate it therapeutically against infection or for apexification purposes. I was a little overzealous with my obturation (warm lateral condensation for this case) and squished out a heavy amount of sealer.

To show you that presence of infection is really the only factor that affects apical healing, I took the third film as a recall this year. The left central incisor has completed apical maturation. The sealer outside the right central is still there but the periapical radiolucent area has practically disappeared. Clinical examination found no signs of infection and our patient reports no issues with the tooth.

This is a healed case.

The goal of my therapy is not to squish sealer out the apex, but to create a favorable environment for osseous healing. I did both of those things here. Extra-radicular material will increase post operative inflammation and will cause a foreign body reaction which can result in a fibrous connective tissue scar. The scar can look like a persistent lesion over time and complicate future diagnosis.

Histology of the periapex (yes, that’s my name) of this tooth would probably show fibrous encapsulation of the sealer, but in this case the capsule is thin enough that it does not show radiographically.

Hey, I’m not perfect and not everything I do works out the way it is supposed to. Fortunately for our patient this case did. Seeing how a substantial Ellis II fracture line is now obvious on the left central, I might see this guy again at some point in the future for work on that tooth.

And lest I forget, one more thing: When you get your cases back from an endodontist and they say that the tooth has been temporized with a cotton pellet and Cavit, please remove the cotton pellet from under the Cavit before you place your permanent filling.

© Periapex for The Periapex, 2008. | Permalink | 10 comments |

As I wrote this I was thinking that the exam candidates could probably quote literature like crazy back at me with respect to dental trauma while here I am slowly forgetting even the classic Andreasen stuff. Oh well, such is life in the fast lane.

Dear Mr. Lawyer,

Thank you for your inquiries regarding XXX (your file No. XXX).

Dental trauma generally leaves involved teeth with a guarded long-term prognosis. This is especially true in luxation injuries (injuries where the tooth is physically displaced in one direction or another and requires repositioning). Delayed sequela of trauma such as internal or external resorption (reduction of root structure), root canal infection, or ankylosis (loss of the tooth’s physiologic attachment apparatus to the jawbone) can become obvious and problematic many years later.

XXX’s tooth 12 currently appears to be in a stable situation and does not demonstrate obvious signs or symptoms associated with infection. This is subsequent to trauma that occurred over three years ago. My testing, however, does provide some evidence consistent with a necrotic (dead) pulp (nerve) within the tooth.

Endodontic (root canal) treatment of a tooth with a necrotic pulp is not essential as a therapeutic measure. Should the pulp become infected, however, endodontic treatment then becomes necessary. The period of time between pulpal necrosis and infection varies from case to case. Generally, the easier it is for bacteria to penetrate into the canal space of the tooth, the faster necrosis will convert to infection.

Because tooth 12 is intact, has no decay, and no pre-existing fillings, the chance of infection developing within the near future is slim. The elective option of pursuing root canal treatment of this tooth for prevention of future potential infection does have some risk associated with it and could actually potentiate other issues with the tooth. I am of the opinion that the tooth should be monitored for problems (through the usual dental recall visits) and any future problems be addressed as needed.

The root canal space within this tooth has become significantly restricted. This is a reactive response of the pulp to the injury before it died off. The more restricted the canal space is, the more complicated root canal therapy becomes and the greater risk of irreparable damage to the tooth whilst searching for an opening into the canal.

At this point the best indicator of retentive potential of the tooth is the external resorption that I observe radiographically. The tip of the root is shorter and more blunted than it should be. This occurred as part of the biologic repair process in the area subsequent to the accident. I have no historic radiographs to compare current ones to, so I am working under the assumption that the resorptive process is currently arrested. If this is not the case and the resorption is in fact progressive, the tooth will be lost once the root is completely resorbed. This is the other reason the tooth needs to be monitored for some time longer at regular recall intervals.

Should this tooth be lost, an osseointegrated dental implant would be the ideal way to replace it. Permanent tooth replacement is best done once jaw growth is complete (generally between 18 and 21 years). Because my expertise lies within the bounds of retaining this tooth, replacement options, costs, and timeline are best discussed with the dentist who would actually perform the replacement procedures.

I hope this information is of value to you. Should you wish to further discuss this case, please feel free to email me at XXX.

Sincerely,

Ameloblast

© Ameloblast for The Periapex, 2007. | Permalink | 3 comments |

Am I too busy, not busy enough, was life more interesting a few months ago when I was posting like mad to the blog?
It’s a combination of all of the above, but most importantly, it’s because of Facebook.

I’ve recognised my problem, admitted it, now I have to change. I’ll waste less time on Facebook, and waste more time posting to the blog. Now I only have to find things to post about…

I’ll think about that once I finish this dento-legal letter to a lawyer asking for a translation to lay terms of a case about a boy who suffered an intrusive luxation injury a few years ago and presented to me for exam a couple of months ago. The lawyer needs to know what the terms ankylosis, calcific canal obliteration, and apical external resorption mean.

© Ameloblast for The Periapex, 2007. | Permalink | 3 comments |

Here’s how I first saw these teeth. There is a blurry history of trauma (kickboxing injuries) and when I first saw the patient there was discharge associated with 22.

This first xray is from August 2nd, 2006.

At this point, 22 looked like it had suffered from incomplete root formation, some external resorption, possibly dens-in-dente, and of course infection. I thought I’d have a rough time locating the canal.

Not so. During treatment, I found a massively large canal that was much, much shorter than where I expected it to end. I cleaned things up as best I could and then loaded the canal up with calcium hydroxide for a couple of weeks (or a month…I can’t remember off hand).

The next xray is from October 11th, 2006. Obturation is obviously short of where the root ends, but electronic apex readings were consistent to this point. This angle also shows that what I thought was a root with a canal was actually just one side of the actual root. I started to worry about some sort of vertical root fracture having split the root up the middle. There was no internal visual evidence of this however, and the medicated phase had cleared up the sinus tract.

Later films will show that that left part of root might actually be a root tip that’s floating around from a horizontal root fracture. I reasoned that the short apex readings were either from a resorptive perforative defect through the root at that level, or because of the blunderbuss apex.

When there’s doubt, I use the apex locator as my diviner of length. Once I can get consistent readings with it, I tend to trust it beyond what my eyes see.

One more thing: I informed that patient that a lesion was now becoming apparent apical to 21.

The next film is from November 8th, 2006. Tooth 22 was doing fine, but another sinus tract had appeared. A sinugram traced it to the apex of 21.

A retreatment with a medicated phase was initiated for the tooth.

The canal was cleared, medicated with calcium hydroxide for a month, and then obturated. The apical canal area was irregularly calcified because of the incomplete root formation and the previous work. That’s still no excuse for the voids in the obturation…But proof of success is always in the pudding.

This xray is from February 26th, 2007. It’s post-obturation of 21.

And this next one is from July 30th, 2007. The lesions are shrinking and trabeculation is becoming apparent within them. I’m still not sure what happened with 22 and I’m not sure at this point what is happening. There’s either some external resorption going on as the bone heals and remodels, or that one thing that looks like a root is a root and it’s moving around…

I’ve been temped to go back into 21 and try to improve the appearance of the apical obturation so that the case is more presentable. That, however, won’t necessarily be serving the patient’s best interest. Healing is occurring, so we know there are no bacteria up there. The remaining obturation is good. Any corrective work would be for my benefit rather than the patient’s.

© Periapex for The Periapex, 2007. | Permalink | 8 comments |

Percussion produced a higher pitched sound on the 3 than the other teeth, and when I checked mobility, there wasn’t even any physiologic movement.

I diagnosed ankylosis, replacement/external resorption, and told the patient to consider replacement options. He’ll probably be ok leaving the tooth alone for now, but if the replacement resorption is still active, he will lose the tooth sooner than later.

These are all things we see with teeth that have been traumatised (avulsed in particular). The only history of “trauma” to this tooth is the RPD…

© Ameloblast for The Periapex, 2007. | Permalink | 4 comments |

This a case of a horizontal root fracture. The endo was done 1.5 years after the accident because no vitality had returned to the tooth and a grey caste was developing. Endo for prevention of infection was advised. Teeth with horizontal root fractures are tough teeth to endodontically treat and once infection sets in, the prognosis becomes even more guarded.

Once I started the endo, I got through necrotic tissue coronally, but as I approached the fracture line, I found vital tissue (was able to tell because of hyperemia). In order to try to preserve as much of this tissue as possible (to help with potential reduction and stabilization of the fracture and also for possible biologic closure of the end of the coronal root fragment–ie. apexification) I minimally instrumented to the fracture and then filled the canal to that point with white MTA (mineral trioxide aggregate).

Two years later, osseous healing is complete and the root segments appear to be stabilized. Mobility has reduced. There’s a cosmetic issue now though. Although I used white MTA and the pt’s dentist bleached the tooth prior to placing the final resin, it’s turning more and more grey. Oh well, at least he still has the tooth.

And speaking of horizontal root fractures, here is a case that I did years ago. I wouldn’t necessarily do the same thing today but the post op film looks cool.

© Ameloblast for The Periapex, 2006. | Permalink | 2 comments |